Autonomic Nervous System Pharmacology Flashcards
6 cards from real Pharmacology practice questions. Tap to flip, then mark Knew It or Still Learning โ missed cards come back until you master them.
Read the first 6 Autonomic Nervous System Pharmacology flashcards as text
A 68-year-old male with benign prostatic hyperplasia (BPH) and hypertension is prescribed a medication that provides relief for both conditions. Which of the following mechanisms of action is most likely responsible for the therapeutic effects of this drug?
Answer: Blockade of alpha-1 adrenergic receptors
Alpha-1 adrenergic antagonists, such as prazosin and doxazosin, block alpha-1 receptors on the smooth muscle of the bladder neck and prostate, which improves urine flow in BPH. They also block alpha-1 receptors on vascular smooth muscle, leading to vasodilation and a decrease in blood pressure, making them effective for hypertension. Beta-1 blockade primarily affects the heart, muscarinic stimulation would worsen urinary symptoms, and acetylcholinesterase inhibition is not a primary treatment for these conditions.
A patient is being treated with a non-selective beta-blocker for hypertension. Which of the following is a potential adverse effect that requires careful monitoring, especially in a patient with a history of respiratory disease?
Answer: Bronchoconstriction
Non-selective beta-blockers, like propranolol, block both beta-1 and beta-2 adrenergic receptors. Blockade of beta-2 receptors in the lungs can lead to bronchoconstriction, which can be dangerous for patients with asthma or COPD. Tachycardia is unlikely as beta-blockers slow the heart rate. While they can mask symptoms of hypoglycemia, bronchoconstriction is a more direct and concerning respiratory effect. Urinary retention is more characteristic of anticholinergic drugs.
An elderly patient is administered atropine as a preanesthetic agent to reduce secretions. Which of the following signs would most likely indicate atropine toxicity?
Answer: Dry mouth, blurred vision, tachycardia, and delirium
Atropine is a muscarinic antagonist. Toxicity, or an anticholinergic crisis, manifests as symptoms that are opposite to the parasympathetic 'rest-and-digest' functions. These include dry mouth (decreased salivation), blurred vision (mydriasis and cycloplegia), tachycardia (blockade of vagal tone), and central nervous system effects like confusion and delirium. The other options describe cholinergic crisis (A, B) or sympathetic overstimulation (C).
A patient in septic shock is administered a continuous infusion of a drug that primarily acts as a potent alpha-1 adrenergic agonist to increase blood pressure. Which of the following drugs was most likely administered?
Answer: Phenylephrine
Phenylephrine is a selective alpha-1 adrenergic agonist that causes potent vasoconstriction of arterioles and veins, leading to an increase in systemic vascular resistance and blood pressure. This makes it useful in cases of vasodilatory shock. Isoproterenol and albuterol are primarily beta-agonists, and dobutamine is a beta-1 agonist, which would primarily increase heart rate and contractility without the potent vasoconstriction needed to reverse septic shock.
Which of the following statements best describes the mechanism of action of pilocarpine when used to treat glaucoma?
Answer: It is a direct-acting muscarinic agonist that increases aqueous humor outflow.
Pilocarpine is a direct-acting cholinergic (muscarinic) agonist. In the eye, it stimulates muscarinic receptors on the ciliary muscle, causing it to contract. This contraction increases the outflow of aqueous humor through the trabecular meshwork, thereby reducing intraocular pressure in glaucoma.
A patient with myasthenia gravis is treated with pyridostigmine. This drug improves muscle strength by what mechanism?
Answer: Reversibly inhibiting the acetylcholinesterase enzyme
Pyridostigmine is a reversible acetylcholinesterase inhibitor. By inhibiting the enzyme that breaks down acetylcholine (ACh), it increases the concentration and duration of action of ACh in the synaptic cleft. This enhanced availability of ACh allows for greater stimulation of the remaining functional nicotinic receptors at the neuromuscular junction, thereby improving muscle strength in patients with myasthenia gravis.